钡诱导的豚鼠心室肌舒张期去极化及其控制机制

Barium-induced diastolic depolarization and controlling mechanisms in guinea pig ventricular muscle.

作者信息

Shen J B, Vassalle M

机构信息

Department of Physiology, State University of New York, Health Science Center, Brooklyn 11203, USA.

出版信息

J Cardiovasc Pharmacol. 1996 Sep;28(3):385-96. doi: 10.1097/00005344-199609000-00007.

DOI:10.1097/00005344-199609000-00007

PMID:8877585

Abstract

Barium-induced diastolic depolarization (Ba(2+)-DD) and its modulation were studied in guinea pig papillary muscle and single ventricular myocytes. In papillary muscles, Cs+ (4 mM) abolished the DD induced by Ba2+ (0.05-0.2 mM) by abolishing the undershoot at the end of the action potential (AP; consistent with a block of an outward current). Acetylcholine (ACh 1 microM) had little effect on Ba(2+)-DD, whereas norepinephrine (NE 1 microM) enhanced it by increasing the undershoot and by inducing an oscillatory potential. Low [Ca2+]o (0.54 mM) decreased the resting potential and increased Ba(2+)-DD amplitude. High [Ca2+]o (8.1 mM) had opposite effects. Cs+ also reduced Ba(2+)-DD in low [Ca2+]o. In isolated myocytes, Ba(2+)-DD and the pacemaker current induced by Ba2+ (Ba(2+)-IKdd) increased on depolarization and reversed on hyperpolarization. Although not significantly, high [Ca2+]o slightly decreased and low [Ca2+]o slightly increased Ba(2+)-IKdd. Cd2+ markedly reduced the slow inward current ICa and the AP duration (APD), but did not affect Ba(2+)-IKdd. We conclude that Ba(2+)-DD (a) is entirely due to a voltage- and time-dependent decrease in gK1, since it is abolished by Cs+ (no contribution of a nonblocked decaying IK) by eliminating the undershoot (no If), (b) is potentiated by NE through an increased undershoot and an oscillatory potential, (c) is modified by high and low [Ca2+]o mostly through changes in the resting potential, and (d) is not affected by the block of the slow channel by Cd2+.

摘要

在豚鼠乳头肌和单个心室肌细胞中研究了钡诱导的舒张期去极化（Ba(2 +)-DD）及其调节机制。在乳头肌中，Cs⁺（4 mM）通过消除动作电位（AP）末期的负后电位（这与外向电流的阻断一致），消除了由Ba²⁺（0.05 - 0.2 mM）诱导的DD。乙酰胆碱（ACh 1 μM）对Ba(2 +)-DD影响很小，而去甲肾上腺素（NE 1 μM）通过增加负后电位和诱导振荡电位来增强它。低[Ca²⁺]ₒ（0.54 mM）降低静息电位并增加Ba(2 +)-DD幅度。高[Ca²⁺]ₒ（8.1 mM）则有相反的作用。Cs⁺在低[Ca²⁺]ₒ时也降低Ba(2 +)-DD。在分离的肌细胞中，Ba(2 +)-DD和由Ba²⁺诱导的起搏电流（Ba(2 +)-IKdd）在去极化时增加，在超极化时反转。虽然不显著，但高[Ca²⁺]ₒ略微降低而低[Ca²⁺]ₒ略微增加Ba(2 +)-IKdd。Cd²⁺显著降低缓慢内向电流ICa和动作电位时程（APD），但不影响Ba(2 +)-IKdd。我们得出结论：Ba(2 +)-DD（a）完全是由于gK1的电压和时间依赖性降低，因为它通过消除负后电位（无If）被Cs⁺消除（无未被阻断的衰减IK的贡献）；（b）被NE通过增加负后电位和振荡电位而增强；（c）主要通过静息电位的变化被高和低[Ca²⁺]ₒ改变；（d）不受Cd²⁺对慢通道的阻断影响。